Mixed pulmonary infection by Aspergillus and Mucorales is a rare condition but highly fatal in immunocompromised hosts. We report a 61-year-old diabetic man with diabetic kidney disease who presented with fever and cough. Bronchoscopy-guided lung biopsy and lavage MUCOR 28S PCR assay confirmed dual invasive Aspergillus and Mucorales coinfection. He developed massive hemoptysis, septic shock, and eventually succumbed despite treatment with antibiotics, liposomal amphotericin B and posaconazole. This case underscores the importance of early diagnosis, antifungal therapy and vigilant monitoring in high-risk patients.

Euglycemic diabetic ketoacidosis (EDKA) is a complication of sodium-glucose cotransporter-2 (SGLT2) inhibitors that is being increasingly documented. It is challenging to diagnose, especially in critically ill patients because hyperglycemia is absent or mild. We report the case of a 71-year-old man with type 2 diabetes mellitus previously treated with dapagliflozin, which had been discontinued 2 weeks before presentation, who was admitted for tracheostomy and percutaneous endoscopic gastrostomy (PEG) placement in the context of a neurodegenerative disorder. On postoperative day 2, he was transferred to the intensive care unit (ICU) for aspiration pneumonia complicated by septic shock. He subsequently experienced recurrent episodes of high anion gap metabolic acidosis associated with positive ketonuria and relative euglycemia. The initial episode was interpreted as mixed septic lactic acidosis and SGLT2 inhibitor-associated EDKA, whereas later episodes were more consistent with isolated recurrent EDKA. Management consisted of treatment of the underlying septic shock, and repeated courses of fixed intravenous (IV) insulin infusions to close the anion gap while maintaining euglycemia. This case demonstrates the importance of suspecting EDKA, especially in critically ill patients on SGLT2 inhibitors who present with unexplained high anion gap metabolic acidosis, even when lactic acidosis is present. Early diagnosis and treatment are essential to prevent complications and relapse.

Sepsis involves dynamic inflammatory and endothelial responses, and the timing of extracorporeal therapies such as therapeutic plasma exchange (TPE) may influence clinical outcomes. However, the optimal timing of TPE remains unclear. This retrospective single-center observational study included adult patients with sepsis or septic shock who underwent TPE in the intensive care unit between January 1, 2017 and August 1, 2025. Patients were categorized as early (≤ 48 hours after diagnosis) or late (> 48 hours). The primary outcome was 28-day mortality. Secondary analyses evaluated longitudinal changes in biomarkers and laboratory parameters. Eighty-eight patients were included (early n = 39; late n = 49). Overall 28-day mortality was 40.9% (36/88). Kaplan-Meier analysis demonstrated no significant difference in 28-day survival between the groups (log-rank P = .91). In multivariable Cox regression adjusted for Sequential Organ Failure Assessment and Acute Physiology and Chronic Health Evaluation II, TPE timing was not independently associated with 28-day mortality (hazard ratio 0.90, 95% confidence interval 0.44-1.83, P = .76). Across the overall cohort, significant temporal changes were observed in C-reactive protein and lactate dehydrogenase levels during TPE treatment. Early TPE initiation was not associated with improved 28-day survival. Observed biomarker trajectories should be interpreted cautiously given the retrospective design, limited sample size, and potential residual confounding.

Streptococcus suis (S. suis) is a zoonotic pathogen that causes severe diseases including meningitis, septic shock, and endocarditis in both pigs and humans. In swine, S. suis is one of the most important bacterial pathogens causing invasive diseases such as meningitis, septicemia, arthritis, and sudden death, with serotypes 1, 2, 7, and 9 being among the most frequently recovered from clinical cases in affected herds across Southeast Asia. We developed a multiplex TaqMan qPCR assay targeting four serotype-specific genes (cps1I, cps2I, cps7L, and cps9J) for detection of major S. suis serotypes in porcine samples. The assay achieved a detection limit of 10 copies/μL for all four target serogroups, amplification efficiencies of 89.64% to 100.42% (R[2] ≥ 0.997), and no cross-reactivity with any of the negative controls, including SS4, APP, HPS, Salmonella, E. coli, and S. aureus. Intra-assay and inter-assay repeatability were below 3%. Testing 98 clinical porcine samples from Guangxi, China, yielded positivity rates of 26.53% for the serotype 1/14 group, 19.39% for the serotype 2/1/2 group, 17.34% for serotype 7, and 29.59% for serotype 9, respectively, with mixed-target detection in 30.61% of samples. This assay enables rapid, reliable detection of major zoonotic S. suis serotypes in porcine samples, though it detects serotypes 1 and 14 as a group, and serotypes 2 and 1/2 as a group, due to capsular locus sequence similarity-a limitation acceptable for surveillance given the high pathogenicity within each group. This tool supports One Health-based veterinary surveillance for zoonotic disease control.

Human adenovirus type 7 (HAdV-7) can cause severe pneumonia and sepsis in children, but the associated host epigenetic and immune alterations remain poorly defined. We profiled peripheral-blood DNA methylation in 11 children with HAdV-7-associated sepsis (6 survivors and 5 non-survivors) and 5 pediatric controls without clinically detectable HAdV-7 infection using reduced representation bisulfite sequencing. Differentially methylated genes were integrated with pediatric septic shock transcriptomic modules from GSE26440, and their cellular distribution and predicted regulatory effects were explored using the single-cell dataset GSE167363 and scTenifoldKnk. We identified 106 genes showing differential methylation across all three pairwise comparisons. Cross-cohort integration prioritized 19 candidate genes, among which TP53INP1 showed preferential expression in B cells in the external sepsis single-cell dataset. In silico perturbation of TP53INP1 was associated with changes in interferon-stimulated and antiviral genes, including TRIM22, IFI44L, and PARP14. These findings identify TP53INP1 as a hypothesis-generating candidate linking HAdV-7-associated whole-blood methylation changes with B-cell regulatory networks observed in an external sepsis dataset. Given the small discovery cohort and absence of experimental validation, the findings are exploratory and require confirmation in independent cohorts.

Objective: To compare the clinical characteristics, healthcare exposures, and antimicrobial susceptibility profiles of pediatric Enterococcus faecium and Enterococcus faecalis infections. Methods: This retrospective study included hospitalized children with E. faecium or E. faecalis isolated from sterile specimens between August 2018 and June 2025. Clinical characteristics and antimicrobial susceptibility were compared. Logistic regression identified factors associated with pathogen species, while negative binomial regression evaluated the association between species and length of hospital stay. Results: Among 167 patients, 98 had E. faecium infection and 69 had E. faecalis infection. No significant annual trend in species distribution was observed. Multi-site infection was more common with E. faecium than with E. faecalis (36.73% vs. 15.94%, p = 0.003). Hematologic malignancy, previous hospitalization, central venous catheterization, immunosuppressive therapy, higher procalcitonin levels, and longer hospitalization were more common in the E. faecium group. In three separate primary logistic regression models adjusted for septic shock, central venous catheterization and hospitalization for ≥14 days before culture positivity were associated with higher odds of E. faecium infection, whereas endotracheal intubation was associated with higher odds of E. faecalis infection. In post hoc sensitivity analyses jointly incorporating these healthcare exposures and either hematologic malignancy or immunosuppressive therapy, only central venous catheterization remained significantly associated with E. faecium infection. E. faecium infection was associated with a 33.8% longer hospital stay (aIRR = 1.338, 95% CI: 1.160-1.543, p < 0.001). E. faecium showed substantially greater resistance to ampicillin and penicillin. Conclusions: Pediatric E. faecium and E. faecalis infections differed in patient profiles, healthcare exposures, antimicrobial susceptibility, and disease burden. Species identification may support clinical assessment and antimicrobial stewardship.

Background and Objectives: Necrotizing fasciitis (NF) is characterized by rapid and aggressive infection of the subcutaneous tissue and fascia, and a high risk of death in case of delay in diagnosis and treatment. Materials and Methods: This 7-year retrospective study (May 2017-May 2024) evaluated 38 patients with upper- and lower-limb NF admitted to the surgery clinic at the County Emergency Hospital in Craiova, Romania. Results: 21.8% of the confirmed NF cases were monomicrobial; Gram-positive strains were predominant, but Gram-negative strains were also involved. The mortality rate was 28.9%; acute kidney injury appears as the only independent risk factor associated with mortality, although in univariate analysis, septic shock and high NLR and INR values were also factors associated with mortality. An increased resistance rate to antibiotics was recorded, with a 32.7% MDR rate; moderate to high resistance to piperacillin + tazobactam, most cephalosporins, most carbapenems (for Gram-negative strains), and quinolones was noted. Conclusions: Multidisciplinary management, comprising intensive medical support, prompt targeted antibiotic therapy, and immediate surgical intervention, was critical for achieving favorable patient outcomes. Increasing antibiotic resistance may alter the prognosis in patients with NF.

Total joint arthroplasty is a surgical procedure with rising global incidence. Although a strong postoperative inflammatory response is necessary for tissue repair following primary arthroplasty, it may prove to be harmful if excessive or prolonged. This could compromise osseointegration, increase pain, and delay the detection of periprosthetic joint infection. This narrative review examines the principal inflammatory pathways activated by primary arthroplasty. Damage-associated molecular patterns produced by injury and cell death, such as High Mobility Group Box 1 Protein, cell-free DNA, extracellular ATP, histones, and heat shock proteins, trigger innate immune activation following surgical trauma. These mediators use inflammasome pathways and pattern recognition receptors to intensify inflammatory signaling. The acute-phase trajectory, characterized by increases in C-reactive protein and erythrocyte sedimentation rate, alongside the role of interleukin-6 as a precursor factor, is examined together with synovial markers to facilitate the differentiation between septic and aseptic inflammation. Cytokine signaling cascades (JAK-STAT, NF-κB, MAPK) and the RANK/RANKL/OPG axis at the bone-immune interface are also considered. This manuscript highlights relevant inflammatory pathways, clinically significant biomarkers, and pathway-guided management strategies to provide an overview of the current research on the biological mechanisms underlying perioperative inflammation in primary arthroplasty. No inflammatory biomarker has yet been validated as a predictor of aseptic loosening.